DVT & Virchow's Triad

There are three factors that are thought to contribute to deep venous thrombosis: endothelial injury, venous stasis, and hypercoagulability. Deep venous thrombosis or blood clots form in the deep veins usually in the legs. Although deep venous thrombosis (DVT) predominantly occurs within the deep veins in the legs, it may also occur in the upper extremities. The deep veins pass through the deep tissues and the muscles.

Muscle contractions (walking, running, activity, etc.) squeeze blood through the deep veins to the heart. The deep veins have valves which prevent the blood from flowing back to the feet and ankles. DVT is the formation of a blood clot (thrombus) within a deep vein. The majority of blood clots that form are small, and they are usually broken down or dissolved. Large clots may form and can block the vein causing the patient to complain of pain and swelling. The clot may detach partially or totally (embolism). Some of the clots may be silent and show no symptoms. The detached blood clot may travel from the deep veins to the heart and then finally lodge itself in the pulmonary artery of the lungs. In some cases, the clot will pass through the heart to the aorta and create emboli in the brain (patent foramen ovale). Virchow’s triad contributes to the development of deep venous thrombosis. One of the triad may contribute more than the others. Platelet dysfunction is not part of the Virchow’s triad. Endothelial injury is secondary to injury, trauma, or surgery. It induces thrombosis. It may occur due to manipulation of fractures, dislocation, or from placement of retractors or pressure on the tissues. Venous stasis will lead to platelet contact with the endothelial lining such as with use of a tourniquet, hypotension, or with knee flexion during surgery. It occurs with impaired mobility in the elderly. Immobility will cause the venous circulation to slow down and the clotting factors in the blood to clump together, ultimately leading to DVT. In my opinion, the most important factor is to prevent a blood clot is by maintaining the patient’s mobility. It is important to get the patient up out of bed and moving around when possible either on their own or with crutches. This is a simple preventative step. Hypercoagulability can be caused by tissue debridement, collagen, fibrinogen, tissue thromboplastin, blood diseases such as Protein S and Protein C deficiency, or actor V Leiden mutation. Risk factors for thromboembolism include history of previous thromboembolism, obesity, malignant disease, immobilization, pregnancy, old age, history of congestive heart failure, or oral contraceptives. Risk factors also include genetic blood diseases or major orthopedic procedure. Up to 60% of asymptomatic DVT in total joint arthroplasty can occur if we do not give the patient prophylaxis. Up to 20% of symptomatic DVT can occur without giving the patient prophylaxis for DVT. Proximal DVT can occur in about 15-25%. Fatal pulmonary embolism can occur up to .05%. Total knee arthroplasty has a high risk of DVT but a lower risk for pulmonary embolism than total hip arthroplasty. When giving prophylaxis for blood clots or DVT, we need to balance the risk of clotting and development of DVT versus the risk of bleeding.

Nabil Ebraheim, MD

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